Cardiovascular disease and COPD: dangerous liaisons?

Abstract

Chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD) frequently occur together and their coexistence is associated with worse outcomes than either condition alone. Pathophysiological links between COPD and CVD include lung hyperinflation, systemic inflammation and COPD exacerbations. COPD treatments may produce beneficial cardiovascular (CV) effects, such as long-acting bronchodilators, which are associated with improvements in arterial stiffness, pulmonary vasoconstriction, and cardiac function. However, data are limited regarding whether these translate into benefits in CV outcomes. Some studies have suggested that treatment with long-acting β2-agonists and long-acting muscarinic antagonists leads to an increase in the risk of CV events, particularly at treatment initiation, although the safety profile of these agents with prolonged use appears reassuring. Some CV medications may have a beneficial impact on COPD outcomes, but there have been concerns about β-blocker use leading to bronchospasm in COPD, which may result in patients not receiving guideline-recommended treatment. However, there are few data suggesting harm with these agents and patients should not be denied β-blockers if required. Clearer recommendations are necessary regarding the identification and management of comorbid CVD in patients with COPD in order to facilitate early intervention and appropriate treatment.

Risk factors of acute cardiovascular events following acute exacerbation period for patients with COPD: a nested case-control study

“…Third, some baseline information in the stable period was de cient, and usage of cardioprotective medications were not fully recorded, liker anti-platelet agents and statins, which might result in biases. [14,35] Fourth, baseline comorbidities were reported by patients themselves and not validated by detailed laboratory tests, which might had recall bias. Fifth, we did not take some useful scales of cardiovascular risk assessment into consideration.…”

“…Traditional risk factors of CVDs might have warning effects, including previous history, hypertension, diabetes, hyperlipidemia and hyperuricemia. In addition, serious side effects of some drugs are chief culprits of CVEs, such as theophylline [14] and widely-concerned uoroquinolones [15]. Relationship between inhaled long-acting bronchodilators and CVDs is still highly debated, for their pharmacological mechanisms are contradictory to therapeutics of cardiac remodeling and heart failure.…”

“…Relationship between inhaled long-acting bronchodilators and CVDs is still highly debated, for their pharmacological mechanisms are contradictory to therapeutics of cardiac remodeling and heart failure. [14] In patients with COPD, new initiation of inhaled bronchodilators was related to short-term elevated severe cardiovascular risk, [16] and adding a second bronchodilators to the previous monotherapy also slightly increased the risk of heart failure in one year. [17] Whereas, dual bronchodilators were proved to improve left ventricular lling by reducing lung hyperin ation.…”

GOLD Reports on Chronic Obstructive Pulmonary Disease (COPD): Evolutions, Revolutions and Controversies

“…In terms of treatment, all guidelines concur in recommending to care for these conditions as in the general population 9 . Importantly, COPD should not be considered as a contraindication to the use of selective beta-blockers when there is a clear cardiovascular indication (ischaemic heart disease, heart failure) 34 . Some observational studies suggested that drugs used in cardiovascular conditions could improve the prognosis of COPD (exacerbations occurrence, survival), even in the absence of cardiovascular disease or risk 35,36 .…”

Comorbidities and medical course in a young patient diagnosed with severe obstructive sleep apnea

“…The mechanisms that underlie the association between COPD and CVDs are not well understood, but several processes are thought to be important and may interact with each other. These include lung hyperinflation, hypoxaemia, pulmonary hypertension, systemic inflammation and oxidative stress, exacerbations, shared risk factors and shared genetics, as well as COPD phenotype (6). Endothelial dysfunction fundamentally contributes to the development of atherosclerosis that finally leads to coronary heart disease (CHD).…”